The hapten-binding myelomas of BALB/c mice provide monoclonal populations of antigen-binding B cells which are responsive to immunoregulatory effectors induced in tumor-bearing hosts. Specific, immunological regulation of myeloma cell proliferation, differentiation and immunoglobulin expression demonstrates many of the features which occur in T cell-mediated regulation of non-neoplastic antigen-binding B cells. Immunoregulation of MOPC-315 cell proliferation and immunoglobulin expression can be induced by: (1)\immune response directed to the idiotypic antigens of M315; and (2)\carrier specific presentation of TNP to the cell surface membrane TNP receptor of MOPC-315 cells in carrier-primed syngeneic hosts. Immunization of BALB/c with M315 induces two distinct suppressor T-cell populations. One population mediates a cytostatic effect on MOPC-315 proliferation, and the other population inhibits M315 synthesis and secretion. In the past year, we have shown that inhibition of synthesis results from a specific and reversible suppression of light chain mRNA expression in MOPC-315 cells. Ongoing studies address the molecular mechanisms that mediate this exquisite regulation of immunoglobulin gene expression in myeloma and hybridoma cells. These studies are likely to contribute to a basic understanding of the immunological regulation of normal and neoplastic B cells and may have implications for the control of human B-cell neoplasms such as multiple myeloma.